Interpreting Your Test Results

The Grifols AlphaKit determines your AAT genotype and phenotype. Your genotype is your genetic makeup. Your genotype combines with environmental factors to determine your phenotype, which is your physical characteristics, such as height, weight or alpha1 level. Learn more about the genotype-phenotype relationship.2

Testing for your genotype is efficient and automated, but it can only identify genes for which specific tests have been made. Testing for your phenotype is the most direct method of identifying Alphas and carriers.

The Grifols AlphaKit also measures AAT levels in your blood. If your level is below 82 mg/dL or 11 micromole/L, you should talk to your doctor.

Here are the more common phenotypes and their corresponding AAT levels.1

Phenotype

AAT Blood Levels

MM (2 normal copies)

20–53 µM | 150–350 Mg/dL

MZ (1 normal copy, 1 abnormal copy)

12–28 µM | 90–210 Mg/dL

SS (2 marginally abnormal copies)

13–27 µM | 100–210 Mg/dL

SZ (1 abnormal copy, 1 marginally abnormal copy)

10–16 µM | 75–120 Mg/dL

ZZ (2 abnormal copies)

2.5–7 µM | 20–45 Mg/dL

NULLNULL (2 nonfunctional copies)

0 µM | 0 Mg/dL

HAVE A GOOD TALK WITH YOUR DOCTOR

It's important to have a productive talk with your doctor. Use this list of questions to ask about Alpha-1. Add questions of your own. Print them out. Bring them to your appointment. Find out more about in the Doctor Discussion Guide

WHAT TO DO IF YOU HAVE ALPHA-1

If you have Alpha-1, find out about your treatment options, learn how to manage it, and discover what it means if you are a carrier. Learn what to do if you're Alpha-1.

IMPORTANT SAFETY INFORMATION

PROLASTIN®-C (alpha1-proteinase inhibitor [human]) is indicated for chronic augmentation and maintenance therapy in adults with clinical evidence of emphysema due to severe hereditary deficiency of alpha1-PI (alpha1-antitrypsin deficiency).

The effect of augmentation therapy with any alpha1-proteinase inhibitor (alpha1-PI), including PROLASTIN-C, on pulmonary exacerbations and on the progression of emphysema in alpha1-antitrypsin deficiency has not been conclusively demonstrated in randomized, controlled clinical trials. Clinical data demonstrating the long-term effects of chronic augmentation or maintenance therapy with PROLASTIN-C are not available.

PROLASTIN-C is not indicated as therapy for lung disease in patients in whom severe alpha1-PI deficiency has not been established.

PROLASTIN-C is contraindicated in IgA-deficient patients with antibodies against IgA due to the risk of severe hypersensitivity and in patients with a history of anaphylaxis or other severe systemic reactions to alpha1-PI.

Hypersensitivity reactions, including anaphylaxis, may occur. Monitor vital signs and observe the patient carefully throughout the infusion. Should hypersensitivity symptoms be observed, promptly stop infusion and begin appropriate therapy. Have epinephrine and other appropriate therapy available for the treatment of any acute anaphylactic or anaphylactoid reaction.

PROLASTIN-C may contain trace amounts of IgA. Patients with known antibodies to IgA, which can be present in patients with selective or severe IgA deficiency, have a greater risk of developing potentially severe hypersensitivity and anaphylactic reactions.

The most common drug-related adverse reaction observed at a rate of >5% in subjects receiving PROLASTIN-C was upper respiratory tract infection. The most serious adverse reaction observed during clinical trials with PROLASTIN-C was an abdominal and extremity rash in 1 subject.

Because PROLASTIN-C is made from human plasma, it may carry a risk of transmitting infectious agents, eg, viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. This also applies to unknown or emerging viruses and other pathogens.